Therefore, in pursuit of such a therapeutic, in the current study, we initiated TfRMAb-TNFR treatment in older 10.7-month-old APP/PS1 mice, as opposed to treatment initiation in younger 6-month-old mice [17], and continued the treatment till the mice were 13 months old, a stage at which we expect the Aβ pathology to plateau in this mouse model to mimic late stages of AD [28]. This evidence concerns the gene TNFRSF1A and Alzheimer disease.